<i>Retracted:</i>Micro<scp>RNA</scp>‐219 decreases hippocampal long‐term potentiation inhibition and hippocampal neuronal cell apoptosis in type 2 diabetes mellitus mice by suppressing the<scp>NMDAR</scp>signaling pathway

Zhang, Ling; Chen, Zheng-Wen; Yang, Shufen; Shaer, Muyasi; Wang, Ying; Dong, Junjie; Jiapaer, Beili

doi:10.1111/cns.12981

Cited by 22 publications

(7 citation statements)

References 40 publications

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“…Diabetes mellitus (DM) increases the risk of central nervous system disease leading to encephalopathy (Sima et al, 2004), because hyperglycemia, the mainly characterized of DM, triggers neuronal damage (Fan et al, 2016; Kumar et al, 2017). Increasing evidence demonstrated that hyperglycemia induces neuronal senescence (Reno et al, 2013; Kaur et al, 2017; Yerra et al, 2017; Zhang et al, 2019). Therefore, increasing the defenses against hyperglycemia-induced neuronal senescence represents a future strategy for diabetic encephalopathy.…”

Section: Introductionmentioning

confidence: 99%

Hydrogen Sulfide Inhibits High Glucose-Induced Neuronal Senescence by Improving Autophagic Flux via Up-regulation of SIRT1

Chen

Wang

et al. 2019

Front. Mol. Neurosci.

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Hyperglycemia, a key characteristic and risk factor for diabetes mellitus (DM), causes neuronal senescence. Hydrogen sulfide (H 2 S) is a novel neuroprotectant. The present work was to investigate the potential effect of H 2 S on hyperglycemia-induced neuronal senescence and the underlying mechanisms. We found that NaHS, a donor of H 2 S, inhibited high glucose (HG)-induced cellular senescence in HT22 cells (an immortalized mouse hippocampal cell line), as evidenced by a decrease in the number of senescence associated-β-galactosidase (SA-β-gal) positive cells, increase in the growth of cells, and down-regulations of senescence mark proteins, p16 INK4a and p21 CIP1 . NaHS improved the autophagic flux, which is judged by a decrease in the amount of intracellular autophagosome as well as up-regulations of LC3II/I and P62 in HG-exposed HT22 cells. Furthermore, blocked autophagic flux by chloroquine (CQ) significantly abolished NaHS-exerted improvement in the autophagic flux and suppression in the cellular senescence of GH-exposed HT22 cells, which indicated that H 2 S antagonizes HG-induced neuronal senescence by promoting autophagic flux. We also found that NaHS up-regulated the expression of silent mating type information regulation 2 homolog 1 (SIRT1), an important anti-aging protein, in HG-exposed HT22 cells. Furthermore, inhibition of SIRT1 by sirtinol reversed the protection of H 2 S against HG-induced autophagic flux blockade and cellular senescence in HT22 cells. These data indicated that H 2 S protects HT22 cells against HG-induced neuronal senescence by improving autophagic flux via up-regulation of SIRT1, suggesting H 2 S as a potential treatment strategy for hyperglycemia-induced neuronal senescence and neurotoxicity.

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Section: Introductionmentioning

confidence: 99%

Hydrogen Sulfide Inhibits High Glucose-Induced Neuronal Senescence by Improving Autophagic Flux via Up-regulation of SIRT1

Chen

Wang

et al. 2019

Front. Mol. Neurosci.

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“…Finally, miR-151-3p, miR-466f, miR-139-5p, miR-219, miR-29b, miR-25, and miR-370 are all linked to diabetes 67,68,69,70,71,72,73 , consistent with the inability to clear glucose, insulin resistance, and elevated insulin in Ad-Tmem120a -/mice.…”

Section: Enhancers and Regulatory Rnas Were Also Altered In Ad-tmem120a -/-Micementioning

confidence: 66%

Genomic loci mispositioning inTmem120aknockout mice yields latent lipodystrophy

Czapiewski

et al. 2021

Preprint

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Little is known about the proteins that direct the highly conserved patterns of spatial genome organisation in fat. Here we report that adipocyte-specific knockout of the gene encoding nuclear envelope protein Tmem120a disrupts fat genome organisation, thus causing a novel lipodystrophy syndrome. Tmem120a deficiency broadly suppresses lipid metabolism pathway gene expression and induces myogenic gene expression by repositioning genes, enhancers and miRNA-encoding loci between the nuclear periphery and interior. Tmem120a-/- mice, particularly females, exhibit a lipodystrophy syndrome similar to human familial partial lipodystrophy FPLD2, with profound insulin resistance and metabolic defects that manifests upon exposure to an obesogenic diet. Interestingly, similar genome organisation defects occurred in cells from FPLD2 patients that harbour nuclear envelope protein laminA mutations. Our data suggest TMEM120A may mediate/instigate novel categories of adipose tissue dysfunction across the adiposity spectrum and provide a new miRNA-based mechanism possibly driving the unexplained muscle hypertrophy in human lipodystrophy.

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“…The Ca 2+ /CaMKII/CREB signaling pathway is a critical signal transduction pathway and is involved in the formation and maintenance of learning and memory in the CNS (38,39). Ca 2+ is a second messenger that participates in a range of physiological and biochemical processes in cells.…”

Section: Discussionmentioning

confidence: 99%

κ‑opioid receptor agonist, U50488H, inhibits pyroptosis through NLRP3 via the Ca²⁺/CaMKII/CREB signaling pathway and improves synaptic plasticity in APP/PS1 mice

Song

Cui

et al. 2021

Mol Med Rep

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Alzheimer's disease (AD) is a progressive neurodegenerative brain disorder with slow onset in most cases. Clinically, dementia associated with AD is characterized by memory disorders, aphasia, executive dysfunction and personality and behavior changes. Currently, treatment strategies attempt to reduce certain symptoms, however there is no cure for AD. The aim of the present study was to identify a novel treatment strategy for AD. Thus, the protective effects of a κ-opioid receptor (KOR) agonist, U50488H on neural damage in AD mice were investigated.

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Retracted:MicroRNA‐219 decreases hippocampal long‐term potentiation inhibition and hippocampal neuronal cell apoptosis in type 2 diabetes mellitus mice by suppressing theNMDARsignaling pathway

Abstract: The findings from this study indicated that the upregulation of miR-219 decreases LTP inhibition and hippocampal neuronal cell apoptosis in T2DM mice by downregulating the NMDAR signaling pathway, therefore suggesting that MiR-219 might be a future therapeutic strategy for T2DM.

Cited by 22 publications

References 40 publications

Hydrogen Sulfide Inhibits High Glucose-Induced Neuronal Senescence by Improving Autophagic Flux via Up-regulation of SIRT1

Hydrogen Sulfide Inhibits High Glucose-Induced Neuronal Senescence by Improving Autophagic Flux via Up-regulation of SIRT1

Genomic loci mispositioning inTmem120aknockout mice yields latent lipodystrophy

κ‑opioid receptor agonist, U50488H, inhibits pyroptosis through NLRP3 via the Ca²⁺/CaMKII/CREB signaling pathway and improves synaptic plasticity in APP/PS1 mice

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Retracted:MicroRNA‐219 decreases hippocampal long‐term potentiation inhibition and hippocampal neuronal cell apoptosis in type 2 diabetes mellitus mice by suppressing theNMDARsignaling pathway

Abstract: The findings from this study indicated that the upregulation of miR-219 decreases LTP inhibition and hippocampal neuronal cell apoptosis in T2DM mice by downregulating the NMDAR signaling pathway, therefore suggesting that MiR-219 might be a future therapeutic strategy for T2DM.

Cited by 22 publications

References 40 publications

Hydrogen Sulfide Inhibits High Glucose-Induced Neuronal Senescence by Improving Autophagic Flux via Up-regulation of SIRT1

Hydrogen Sulfide Inhibits High Glucose-Induced Neuronal Senescence by Improving Autophagic Flux via Up-regulation of SIRT1

Genomic loci mispositioning inTmem120aknockout mice yields latent lipodystrophy

κ‑opioid receptor agonist, U50488H, inhibits pyroptosis through NLRP3 via the Ca2+/CaMKII/CREB signaling pathway and improves synaptic plasticity in APP/PS1 mice

Contact Info

Product

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κ‑opioid receptor agonist, U50488H, inhibits pyroptosis through NLRP3 via the Ca²⁺/CaMKII/CREB signaling pathway and improves synaptic plasticity in APP/PS1 mice